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. Author manuscript; available in PMC: 2023 Jul 1.
Published in final edited form as: Prog Retin Eye Res. 2022 Jan 4;89:101039. doi: 10.1016/j.preteyeres.2021.101039

Figure 9. VIP accelerates diabetic wound healing and nerve regeneration in healing corneas through VIPR1.

Figure 9.

(A) NL corneas were pretreated with VIPR1 antagonist or PBS and diabetic corneas with recombinant VIP or BSA as the control 4h prior to epithelial debridement. At 0h, the corneas were wounded by epithelium-debridement (2 mm diameter). At 22 hpw, the remaining wounds were stained with fluorescein and photographed. The wound sizes were calculated and presented as percent of healed area over the size of original wounds. (B) Another set of mice were allowed to heal for 3 days and the corneas were processed for WMCM with beta-tubulin III staining for nerve fibers and endings. The images of whole corneas (upper panels) and high-magnification images of central area (bottom panels) were shown. The Figure shows that VIP regulates epithelial wound healing and nerve regeneration in the corneas, suggesting a therapeutic potential for these molecules in treating diabetic keratopathy. (C) The expression of NGF in wounded, with unwounded (●) as the control, NL or DM corneas treated with (▲) or without VIP antagonist (■). (D) The expression of CNTF in wounded, with unwounded (●) as the control, NL or DM corneas treated with (▲) or without VIP antagonist (■). VIP antagonist suppresses and exogenous VIP promotes wound-induced NGF and CNTF expression in NL and DM corneas, respectively. This figure was originally published in (Zhang et al., 2020a).